Although the role of cathepsin B in GBM has yet to be elucidated, its role in mediating tumor invasion through its proteolytic actions on the extracellular matrix has been proposed (35), while more recent findings suggest that cathepsin B may be critical in imbuing these glioma initiating cells with a stem cell-like phenotype, with characteristics including aberrant self-renewal and proliferation, through upregulation of SOX2 and Bmi1 (36). This evidence concerns the gene BMI1 and glioma.